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Endocrine Two > Konorev - Corticosteroids > Flashcards

Konorev - Corticosteroids Flashcards

1
Q

Adrenal CS act where?

A

they are ligands at nuclear receptors, translocate from cytoplasm to nucleus.

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2
Q

MC target cells where?

A
  • Kidney: cells in principal cells of DcT and CD.

- Heart and vasculature: non-epithelial tissue

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3
Q

Action of MC in kidney.

A

Increase Na reabsorption/water retention.

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4
Q

Excess aldosterone (MC) adverse effects on heart and effects on vasculature.

A
  • Cardiac fibrosis and hypertrophy

- Vascular remodeling and inflammation

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5
Q

Decreased activity (inactivating mutations) of what enzyme will cause excessive activation of MR mediated by cortisol to cause HTN and edema?

A

11beta-hyroxysteroid dehydrogenase, type 2

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6
Q

Two steroids that bind to MC-receptors with similar affinity?

A

aldosterone and cortisol

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7
Q

What converts cortisol into inactive cortisone?

A

11beta-hyroxysteroid dehydrogenase, type 2

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8
Q

Excessive activation of MR by cortisol causes what adverse effects?

A

HTN and edema

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9
Q

Three metabolic effects of excess GC

A
  1. Carbohydrate metabolism decrease - development of hyperglycemia
  2. Lipid metabolism increase - development of change in fat distribution (thinning of arms/legs; accumulation in upper body)
  3. Protein metabolism increase - myopathy and muscle wasting
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10
Q

GC interact with insulin in what way?

A

ANTI-INSULIN ACTIONS. Change gene expression in favor of lipolysis and protein breakdown = increased substrates for gluconeogenesis and HYPERGLYCEMIA.

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11
Q

effect GC has inflammation

A

decrease inflammation

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12
Q

effect GC has on immune system

A

immune suppression and decreased allergic hypersensitivity reactions.

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13
Q

A person has Addison’s Disease and needs replacement therapy - what combination of corticosteroids should be administered?

A

GC (hydrocortisone) + MC (fludrocortisone)

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14
Q

What three broad categories are clinical indications for CS administration?

A
  1. Replacement therapy
  2. Immunosuppression (transplant or immune disease)
  3. Inflammatory/allergic conditions (asthma, RA, IBD, etc)
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15
Q

AE of MCs (Fludrocortisone)

A

(AE of aldosterone)

  • Na/H2O retention = edema, HTN
  • Increased preload and hypertrophy of heart = CHF
  • K+ loss and alkalosis
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16
Q

AE of GCs

A

hyperglycemia, suppressed ability to fight infections, muscle wasting and myopathy, development of striae, easy bruising, hypertension, osteoporosis, peptic ulcers, increased appetite and weight gain, retarded growth in children, glaucoma, psychiatric symptoms (euphoria, mania, anxiety)

17
Q

Goals for CS dosing/admin.

A
  • Shortest, fastest, smallest distribution and duration.

- TAPER

18
Q

Do not give GC in pts with:

A
  • Diabetes (hyperglycemia)
  • Immunocompromised or with infections (suppressed ability to fight infections)
  • Children (retarded growth)
  • Psych conditions (euphoria, mania, anxiety)
  • Cardiovascular conditions (HTN, CHF, Angina)
  • Osteoperosis (post-menopausal)
  • Peptic ulcers
19
Q

Aminoglutethimide - Drug class, MOA

A
  • Drug class: Steroid synthesis inhibitor

- MOA: blocks conversion of cholesterol to pregnenolone&raquo_space; reduces production of all steroid hormones

20
Q

Aminoglutethimide - Clinical indications, AE

A
  • Clinical indications: breast cancer tx (historical), adrenocortical cancer
  • AE: GI upset, drowsiness
21
Q

Ketoconazole - Drug class, MOA

A
  • Drug class: steroid synthesis inhibitor

- MOA: inhibits CYP450s; reduces synthesis of adrenal and sex hormones

22
Q

Ketoconazole - Clinical indications, AE

A
  • Clinical indications: antifungal; Cushing’s syndrome; suppression of androgenic hair loss; prostate cancer
  • AE: hepatotoxicity, gynecomastia
23
Q

Metyrapone - Drug class, MOA

A
  • Drug class: steroid synthesis inhibitor

- MOA: inhibits 11-hydroxylation of steroids, selectively suppresses cortisol and cortisone production

24
Q

Metyrapone - Clinical indications, AE

A
  • Clinical indications: Cushing’s Syndrome (esp PREGNANT women)
  • AE: Na/H2O retention and hirsutism in women (due to accumulation of 11-deoxycortisol); GI upset, dizziness
25
Q

Mitotane - Drug class, MOA

A
  • Drug class: steroid synthesis inhibitor
  • MOA: blocks Na and Ca channels; inhibits protein kinase C and adenylyl cyclase > nonselective cytotoxic action on adrenal cortex
26
Q

Mitotane - Clinical Indications and AE

A
  • Clinical Indications: adrenal carcinoma

- AE: depression, somnolence; GU upset (N/V/D); rash

27
Q

Mifepristone - Drug class and MOA

A
  • Drug Class: GC antagonist
  • MOA: stabilizes chaperone proteins (hsp90) on glucocorticoid receptor complex in the cytosol and prevents translocation to the nucleus; antagonist at progesterone receptors
28
Q

Mifepristone - Clinical Indications and AE

A
  • Clinical Indications: hypercortisolism in adults with Cushing’s syndrome; ABORTIONS
  • AE: dizziness, GI upset (nausea/anorexia/vomiting), fatigue
29
Q

Spironolactone - Drug class and MOA

A
  • Drug class: aldosterone antagonist

- MOA: Aldosterone receptor antagonist; also some antagonism of androgen receptors

30
Q

Spironolactone - Clinical Indications and AE

A
  • Clinical Indications: primary hyperaldosteronism, hirsutism in women, K-sparing diuretic (HF and HTN)
  • AE: hyperkalemia; gynecomastia and impotence in men; menstrual abnormalities in women
31
Q

Eplerenone - Drug class and MOA

A
  • Drug class: aldosterone (MC) antagonist
  • MOA: antagonist of aldosterone at the mineralocorticoid receptor; some androgen receptor antagonism, but less than spironolactone
32
Q

Eplerenone - Clinical Indications and AE

A
  • Clinical Indications: HTN, HF

- AE: hyperkalemia

33
Q

CS binding to TRANSCORTIN/CBG (corticosteroid binding globulin) has a high affinity in what two states. Low affinity in what state? (free:protein bound drug)

A

Low affinity during LIVER DISEASE (increased free-protein-bound drug)
High affinity during PREGNANCY or HYPERTHYROIDISM (decreased free-protein-bound drug)

34
Q

When is transcortin saturated?

A

When plasma cortisol exceeds 20-30micrograms/dL.

35
Q

1/2 life of cortisol is increased in what two cases?

A

liver diseases and hypothyroid. Why? Because cortisol is metabolized by the liver. Transcortin is produced in the liver.

36
Q

11beta-hyroxysteroid dehydrogenase, type 2 converst CORTISOL into inactive MR cortisone in kidney, salivary glands, sweat glands, colon epithelium, resulting in what?

A

Making them MC responsive.

37
Q

What could result in inhibition of 11beta-hyroxysteroid dehydrogenase, type 2?

A
  • Apparent MC Excess Syndrome (AME)

- glycyrrhizin (active ingredient in licorice root) –> HTN

38
Q

cortisol/cortisone ratio is ____ in urine in AME.

This syndrome results in what?

A
  • increased

- excessive activation of MR mediated cortisol (bc cannot be inactivated to cortisone)

39
Q

Drugs with both MC and GC actions.

A

hydrocortisone, cortisone, prednisone, methylprednisolone, fludrocortisone

Endocrine Two (16 decks)

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